ACC atrial fibrillation guidelines 2023

 A few key points from the 2023 atrial fibrillation guidelines American College of Cardiology

New classification: 

The old classification is maintained but it is encompassed in a broader classification outlining the stages of risk and /or the occurrence of atrial fibrillation. 

Stage 1:  at risk. This refers to the presence of risk factors such as obesity and hypertension. 

Stage 2: pre atrial fibrillation encompassing structural abnormalities such as LAE or warning arrhythmias such as  atrial ectopy.

Wiithin atrial fibrillation itself the traditional categories of paroxysmal persistent and permanent remain. Right above permanent atrial fibrillation is another designation referring to successful ablation. 

Flexibility is built into the CHA₂DS₂-VASc score for anticoagulation decisions. 

If the risk is intermediate there is considerable equipoise and shared decision making is advised. 

Increased preference for early rhythm control.

There is an increased emphasis on early rhythm control especially in patients with heart failure and reduced ejection fraction. Catheter ablation via pulmonary vein isolation now he has a class 1 indication particularly in patients with who present with heart failure and reduced ejection fraction at the time of the onset of atrial fibrillation detection.   Specifically:

Rhythm control recommended over rate control if decreased left ventricular function and persistent or high burden atrial fibrillation, class 1 

If atrial fibrillation is symptomatic, class 2a. 

Specific arrhythmias related to fibrillation have been defined. 

Atrial tachycardia is defined as a rate greater than or equal to 100, non sinus. Mechanisms can be automaticity, triggered or micro reentry  Atrial flutter. is considered any tachyarrhythmia  that involves macro re-entry. Typical flutter involves macro reentry that goes through the cavo tricuspid isthmus. All others are considered atypical.

Caffeine avoidance is noted not to be beneficial. 

The designation of valvular versus non-value or atrial fibrillation has become obsolete. 

The recommendation now is that for a mechanical prosthesis or severe rheumatic mitral stenosis warfarin is recommended.  DOACs are preferred for all other patients unless there are certain disease-related or pharmacokinetic contraindications. 

In cases of cryptogenic stroke there is a 2a recommendation for extended monitoring. The guidelines do not specify the duration of monitoring. 

For device detection of high rate episodes, (specifically pacemaker detection), stroke risk is believed to exist but believed to be less than that of clinical episodes. 

If a high rate episode is detected and lasts greater than or equal to 5 minutes it is almost always atrial fibrillation. For device detection of high rate episodes lasting greater than or equal to 24 hours systemic anticoagulation is given a 2a recommendation.   For the range of 5 minutes to 24 hours this same situation has a 2b recommendation. In both cases there is considered to be sufficient equipoise that shared decision making applies.

Atrial appendage occlusion devices such as the Watchman have a 2a recommendation if CHA₂DS₂-VASc  is greater than or equal to 2 and anticoagulation is contraindicated. 

For high bleeding risk but not a contraindication the device is given a 2b recommendation. 

There are some changes in systemic anticoagulation recommendations for varying degrees of kidney disease. 

Up to and including stage 3 systemic anticoagulation if otherwise recommended for atrial fibrillation has a class 1 recommendation. It drops to class 2a for stage 4 and to 2B if there is  esrg/hd. 

In atrial fibrillation with rheumatic valve disease or mechanical prosthesis for which vitamin K antagonist anticoagulation is recommended the CHA₂DS₂-VASc  score does not apply. 

The long-term rate control goal is an upper rate limit of 100-110 and has a 2a recommendation. 

Acute rate control

If EF is greater than 40, IV beta blocker or non-dihydropyridine calcium blocker, class 1.  Digoxin  if above ineffective or contraindicated class 2a. 

IV mag sulfate class 2a. It may be better than standard agents. Up to five grams is considered low dose. Occasionally one could use greater than or equal to 5 g.  The main use is adjunctive.

Amiodarone if others ineffective or contraindicated, class 2b.

AVN ablation indications

AV node ablation if rate control is refractory to medication and the patient is otherwise a candidate, 2a. This will be combined with pacing obviously and initial lower rate limit, to avoid malignant ventricular arrhythmia, should be set at 80 to 90 with plans to program down by monthly decrements of 10 until 60 is reached. 

 Stroke prevention associatied with cardioversion 

 If atrial fibrillation could have been going on greater than or equal to 48 hours 3 weeks of anticoagulation first or tee prior to cardioversion and anticoagulation for greater than or equal to 4 weeks afterwards. 

 Drugs to maintain sinus rhythm long-term. 

The guidelines are not very explicit about whether drugs should even be used in the first place. They merely say that such are “ reasonable “  for patients who are " not candidates for, or decline” ablation. Similarly those who prefer antiarrhythmic therapy to ablation are considered reasonable candidates. The implication is that you should probably do something to maintain sinus rhythm. 

If normal EF and no structural heart disease and no coronary disease then fleccanide or propofanone 2a

Dronedarone 2a if no recent decompensated HR and if HF class II or better.

Dofetilide 2a if no long QT or torsades risks and no hypokalemia or hypomag, or tendency thereto.

Amiodarone  is 2a but the agents above may be preferable. 

Sotalol is 2b with the same precautions that apply to dofetilide. 

In pts with prior MI, structural disease or EF less than or equal to 40% no recent decompensation or functional class III or worse, dronedarone is 2a.

When does antiarrhythmic therapy need to be administered in the hospital?  And for how long?

Dofetilide 3 d

Sotolol, admit to hospital but the guideline does not specify how long.

ICs:  Observe at least after the first dose.

PVI catheter ablation (pulmonary vein isolation ):

if antiarrhythmics not tolerated, contraindicated or not preferred, class 1.  For younger patients with no or few comorbidities class 1 as  first line even if the atrial fibrillation is paroxysmal. 

For atrial flutter, class 1 ( it would be implied that this is typical flutter ). For a new diagnosis of atrial fibrillation in heart failure with reduced ejection fraction both at the same time early rhythm control is class 1 and ablation is said to be “ beneficial when appropriate” class 1. 

Updated atrial fib guidelines: the essentials

 

From Joseph S.Alpert.

Oral agents for type 2 diabetes: ACP guidelines

From the Annals:

Recommendation 1:

ACP recommends that clinicians prescribe metformin to patients with type 2 diabetes when pharmacologic therapy is needed to improve glycemic control. (Grade: strong recommendation; moderate-quality evidence)

Recommendation 2:

ACP recommends that clinicians consider adding either a sulfonylurea, a thiazolidinedione, an SGLT-2 inhibitor, or a DPP-4 inhibitor to metformin to improve glycemic control when a second oral therapy is considered. (Grade: weak recommendation; moderate-quality evidence.) ACP recommends that clinicians and patients select among medications after discussing benefits, adverse effects, and costs.

Appendix table 1 has a nice summary on outcomes.

New alcoholic liver disease guidelines from the American College of Gastroenterology

Free full text available.

The document is worth reading in its entirety, but there were a few points I found particularly noteworthy:

Patients who are obese should not consume any ethanol at all!

Definitions, from the paper:

Alcoholic fatty liver disease is diagnosed in a patient with AUD with hepatic steatosis on ultrasound and/or elevation in liver enzymes (aspartate aminotransferase (AST) greater than alanine aminotransferase (ALT)), serum bilirubin less than 3 mg/dL, and the absence of other causes of liver disease.

Clinical diagnosis of AH is determined in a patient with rapid development or worsening of jaundice and liver-related complications, with serum total bilirubin greater than 3 mg/dL; ALT and AST elevated greater than 1.5 times the upper limit of normal but less than 400 U/L with the AST/ALT ratio greater than 1.5; documentation of persistent heavy alcohol use until 8 weeks before onset of symptoms; and exclusion of other liver diseases

Baclofen to help patients stop drinking has a conditional recommendation:

In patients with ALD, baclofen is effective in preventing alcohol relapse (Conditional recommendation, low level of evidence).

Pentoxifylline is no longer recommended for severe alcoholic hepatitis. Steroids still are.

At 7 days into steroid therapy the Lille score should be used to determine if the steroids should be continued:

Response to treatment with corticosteroids should be determined at 7 days using the Lille score. Treatment should be discontinued among non-responders to therapy, defined as those with a Lille score greater than 0.45.

The guideline authors acknowledge evidence that N-acetylcysteine infusion in combination with steroids may be associated with improved outcomes in AH. However, they do not feel the evidence is sufficiently strong to justify a guideline recommendation.

Antibiotic therapy is still recommended as part of the overall treatment regimen for variceal bleeding:

Management of the acute variceal bleeding episode involves pharmacological therapy with available vasoactive agents (terlipressin or octreotide), antibiotics, and endoscopic therapy. Endoscopy should ideally be carried out at least 30 min after initiation of vasoactive therapy (54).

As for the optimal timing of endoscopy, that last sentence is confusing to me.

Have a low threshold for starting broad spectrum antibiotics in AH patients who become critical.  

Concerning the gram negative component of the regimen, the guideline recommends merropenem or zosyn, acknowledging that the clinician should pay attention to local sensitivity patterns:

The choice of antibiotics depends on prevailing local antimicrobial resistance patterns. Piperacillin-tazobactam is generally the preferred drug used for sepsis, although vancomycin and meropenem may be considered in patients with penicillin hypersensitivity.

There’s much more.

Can someone explain to me why I need AHRQ?

According to this Kevin MD post we'll all suffer if it becomes marginalized anymore than it already is. I've never used it. What am I missing?

A recent review of the latest Surviving Sepsis guidelines suggests that we go back to early goal directed therapy

Though not in those exact words.

ACP puts out its own guideline for hypertension in the elderly

---and teams up with AAFP.

In short, the target is systolic below 150, and consider below 140 if high cardiovascular risk is present.

As to the choice of pharmacologic agents they don’t write anything in stone:

Effective pharmacologic options include antihypertensive medications, such as thiazide-type diuretics (adverse effects include electrolyte disturbances, gastrointestinal discomfort, rashes and other allergic reactions, sexual dysfunction in men, photosensitivity reactions, and orthostatic hypotension), ACEIs (adverse effects include cough and hyperkalemia), ARBs (adverse effects include dizziness, cough, and hyperkalemia), calcium-channel blockers (adverse effects include dizziness, headache, edema, and constipation), and β-blockers (adverse effects include fatigue and sexual dysfunction).

Focused update incorporating ARNI and ivabradine into the heart failure guidelines

This was recently published in JACC. It applies to heart failure stage C class II and III. It calls for substitution of ARNI for the ACEI or ARB (class I recommendation) and adding on ivabradine in patients on optimal medical therapy but in whom maximal titration of the beta blocker (to blood pressure tolerance) still leaves them with a resting heart rate of 70 or greater (class IIa recommentation). The ARNI substitution has a mortality benefit over the use of ACEI or ARB alone. The ivabradine add on reduces hospitalizations. The recommendation for both applies only to systolic dysfunction heart failure (HFrEF). According to the wording of the guideline update ARNI substitution is an alternative. That is, it, the use of ACEI and the use of ARB all carry a class I recommendation.

Links below contain the prescribing information for the currently approved ARNI and ivabradine, respectively.

Entresto

Corlanor

The new CHEST guidelines for antithrombotic therapy

This go round the update is being handled a bit differently it would seem, by releasing one section at a time.  As of now only the section on VTE treatment has been posted, and the full text can be accessed here.  The rest of the guidelines, e.g. those for antiplatelet therapy and VTE prevention, will, I'm guessing, be posted later, a section at a time.

Retired Doc has already written a nice summary post which you can access here.

For my own take, I'll highlight the major changes and comment on some other points of particular interest.  In this edition as in previous ones the authors are true to the first principle of evidence based medicine (EBM) which is that the ultimate decision maker for treatment is the patient, providing he or she wants to be, as opposed to some pathway, core measure or central controlling authority.  This is illustrated by phrases throughout the paper, often used after their recommendation statements, to the effect that the patient may choose this over that treatment.  The document is well referenced and the recommendations seem based on careful consideration of the evidence.  Those good things being said, the paper is also a masterpiece of obfuscation, examples of which I will point out along the way.  Although there is some sense to be made of it (as I try to provide in plain language below) the process of doing so was very difficult.  The guideline is worth reading in the original text but do so when you are rested, fed and have plenty of time.


The 2012 definitions for duration of therapy are maintained.

Somewhere along the line, in 2012 I believe, the guideline authors changed the category definitions for VTE treatment duration.  They have now been around for a while but, I believe, still confuse clinicians.  The old classification seemed pretty straightforward:  short term (3 months, mainly for patients with transient risk factors), usual (6 months, appropriate for most patients with spontaneous events) and indefinite (potentially for the rest of the patient's life, for those with especially high risk of recurrence).   But the current classification turns that all around.  “Long term” is now defined as 3 months of treatment.  The middle category, “longer, time limited” is defined as 6-12 months.  The third category, termed “extended,” could be any time of longer than 3 months but without a scheduled stop date.  At the risk of pushing this to absurdity extended treatment could be as little as 3 months and one day, meaning that the order of this listing is not necessarily in order of treatment duration though it is implicit in the discussions in the paper that “extended” usually means longer than a year.


So what are the recommended durations of treatment for various clinical circumstances?

For VTE (for purposes of this post that means DVT and/or PE) not associated with active cancer and associated with a transient risk factor, surgical or otherwise, the guideline calls for 3 months treatment.  The strength of the statement (we recommend versus we suggest) varies with bleeding risk but the guideline always prefers 3 months over longer time limited or extended. 

For VTE not associated with active cancer and not associated with a transient risk factor, the order of preference for duration is extended preferred over 3 months which in turn is preferred over longer time limited (see the one exception below).  It is really difficult to make sense of this when, in plain language, it says “potentially for the rest of your life” is choice number 1, 3 months is choice number 2 and 6-12 months is choice number 3.  That is, the descending order of preference does not equal the descending order of duration!  The exception is that if the bleeding risk is high (I'll explain how the guideline defines that later) 3 months of treatment is the preference over the other two options.

To add to the confusion (and perhaps the entertainment value) of the guideline check out this statement from section 9 regarding the decision making process for patients who are potential candidates for extended (as opposed to 3 month) treatment:

Patient sex and D-dimer level measured a month after stopping anticoagulant therapy may influence the decision to stop or extend anticoagulant therapy..

But a month after stopping, well, you've already stopped!  It's almost comical when you think about it.  The plain language version would be stop treatment, wait a while, then run a test to see if you should stop.  What they really must have meant was stop treatment, wait a while, then run a test to see if you should have stopped.  It seems the authors didn't say what they really meant, perhaps because that would have sounded as though they were recommending you put the patient at undue risk.  But I do think there is a basis for this.  The body of the paper cites evidence.  I will appeal to pathophysiology and attempt to explain it this way.  While the patient is systemically anticoagulated the coagulation system is held at bay.  Once you stop, there are certain higher risk patients who will reactivate their coagulation systems in a subclinical manner, with the process simmering beneath the surface.  Such patients, identified by an elevated D dimer, would be considered poised to clot again soon.  So, in certain circumstances, the D dimer may be a useful decision tool.  But what is gender specific about it, as implied in the indented text above?  More from the guideline on that:

..patient sex and D-dimer level measured about 1 month after stopping anticoagulant therapy can help to further stratify the risk of recurrent VTE. 66-69  Men have about a 75% higher (1.75-fold) risk of recurrence compared with women, whereas patients with a positive D-dimer result have about double the risk of recurrence compared with those with a negative D-dimer, and the predictive value of these two factors appears to be additive. The risk of recurrence in women with a negative posttreatment D dimer appears to be similar to the risk that we have estimated for patients with a proximal DVT or PE that was provoked by a minor transient risk factor (approximately 15% recurrence at 5 years); consequently, the argument for extended anticoagulation in these women is not strong, suggesting that D-dimer testing will often influence a woman’s decision. The risk of recurrence in men with a negative D-dimer is not much less than the overall risk of recurrence that we have estimated for patients with an unprovoked proximal DVT or PE (approximately 25% compared with approximately 30% recurrence at 5 years); consequently, the argument for extended anticoagulation in these men is still substantial, suggesting that D-dimer testing will often not influence a male’s decision.

For patients without active cancer who have had two or more spontaneous events the recommendations are the same as for patients with a single spontaneous (ie no transient risk factor) event.

For patients with active cancer extended therapy is favored for all, although the strength of the recommendation varies with bleeding risk. 

No special consideration is given for other high risk situations (eg thrombophilia, clots in unusual places).

Finally, the guideline says that if systemic anticoagulation is stopped for any reason aspirin, absent a contraindication, is considered better than nothing, making the special point that aspirin is not an acceptable alternative for extended systemic anticoagulation.


Choice of anticoagulant:  it's complicated.

The recommendation summary is simple enough but there are many nuances.  In general, for VTE in non-cancer patients the order of preference of agents is a NOAC over warfarin.  The authors give no order of preference among the NOACs.  Concerning initiation of treatment:

Initial parenteral anticoagulation is given before dabigatran and edoxaban, is not given before rivaroxaban and apixaban, and is overlapped with VKA therapy.

There are exceptions to be noted, mainly in unstable patients, for the recommendation not to start with parenteral anticoagulants before administration of some of the NOACs listed above.

For VTE patients with active cancer LMWH is recommend over all the others for initial and long term treatment and, by implication, extended treatment.  There is no order of preference for any of the ones after LMWH (orals). 

Now for the nuances that apply to certain special situations, from table 6:

If the patient has liver disease sufficiently severe to alter the coag tests LMWH is indicated for all phases of treatment.  Two reasons are stated for this, one being that NOACs are contraindicated if the INR is raised by liver disease, and the other being that warfarin is difficult to control in such circumstances and its monitoring is confounded since when the INR is altered by liver disease it is not a reliable indicator of antithrombotic effect.

Renal impairment with clearance below 30 is considered a contraindication to all NOACs for treatment of VTE in the guideline even though the product labeling of some of them allows usage with such reduction in renal function.

Dabigatran is not recommend if the patient has CAD, dyspepsia or prior history or GI bleeding (even if remote).

Similarly rivaroxaban and edoxaban are not recommend if there has been GI bleeding.

If there is concern for poor compliance, warfarin is favored over the NOACs, since it can be detected in the lab and its consequences are not immediate.

Unfractionated heparin is favored for initial treatment if thrombolytics are used or are being considered.

I checked Up to Date regarding the choice of anticoagulant and found that it is more conservative, favoring the traditional approach over starting with a NOAC.


Distal leg DVT.

The recommendations for distal leg DVT are essentially the same as those for proximal DVT except for the acknowledgment that clinical judgment will dictate withholding treatment in some patients.  The guideline “suggests” such a strategy of withholding treatment if there are not severe symptoms or risk factors for recurrence.  In such patients serial imaging is recommended. 



Catheter directed (regional) thrombolysis is not recommended.

The authors imply that it is worthy of consideration in certain circumstances but come short of making even a soft recommendation:

Patients who are most likely to benefit from CDT (see text), who attach a high value to prevention of PTS, and a lower value to the initial complexity, cost, and risk of bleeding with CDT, are likely to choose CDT over anticoagulation alone.

An exception to this non-recommendation is “impending venous gangrene.”  Another exceptional situation, May Thurner syndrome, is not addressed.

(Note: this applies to both upper and lower extremity DVT).


The guideline finds no indication for IVC filter insertion in any patient who can be anticoagulated.

---which is another way of saying that they would recommend an IVC filter only for patients with acute VTE and an absolute contraindication to anticoagulation.  Acknowledging low level data in favor of combined anticoagulation and IVC filter insertion in patients whose PE is severe or unstable (variously defined) the guideline makes this statement:

However, because it is uncertain if there is benefit to placement of an IVC filter in anticoagulated patients with severe PE (eg, with hypotension), and this is done by some experts, our recommendation against insertion of an IVC filter in patients with acute PE who are anticoagulated may not apply to this select subgroup of patients.

Thus the guideline gives little support for IVC filter insertion in any but the strictest indications, which may be important in light of the current FDA Safety Communication on filters and the resulting flurry of legal actions.


What about compression stockings?

Although the guideline authors acknowledge that they may be useful to control leg swelling they are no longer recommended for the singular purpose of prevention of post thrombotic syndrome.


Some small pulmonary artery filling defects may not need to be treated at all.

How is this determined?  Here's the recommendation:

In patients with subsegmental PE (no involvement of more proximal pulmonary arteries) and no proximal DVT in the legs who have a (i) low risk for recurrent VTE (see text), we suggest clinical surveillance over anticoagulation (Grade 2C), and (ii) high risk for recurrent VTE (see text), we suggest anticoagulation over clinical surveillance..

As simple as this sounds it requires some elaboration.  Unanswered questions include: 1)  are they talking about a single subsegmental defect or can treatment be withheld in some cases of more than one?  2)  Is the recommendation based on the idea of a false positive (non VTE filling defect), or that such low clot burdens, even if real, don't require treatment, or both?  The discussion in the body of the paper talks around these issues but is not definitive on either one.  Suffice it to say the recommendations leave much to clinical judgment and patient preference.  Despite such ambiguity in the text here is my take:


The text contradicts itself on whether treatment can ever be withheld in real subsegmental PEs however tiny the clot burden.  However, from the explanatory text it can be inferred that all filling defects judged to be “real” should be treated since such a determination is a risk factor for progression.

Subject to variations based on bleeding risk, patient preference and other clinical judgment factors, for treatment to be withheld ALL the following conditions must be met:

The defect is single.

The CT angio leaves doubt about whether the filling defects really represent PE (ie false positive is likely).

The filling defect is distally situated in a subsegmental branch.

The patient is asymptomatic (usually meaning that the discovery of the filling defect was incidental).

Clinical pretest probability is low or intermediate.

The D dimer is normal or minimally elevated and the elevation is otherwise explained.

The patient is not hospitalized already.

The patient has no recent history of immobility.

The patient does not have active cancer.

The patient has good cardiopulmonary reserve.

DVT is ruled out by lower extremity ultrasound (the upper extremity should also be evaluated if there are risk factors such as lines).

Again this is just my attempt to make sense of the text of this portion of the guideline, which is in places ambiguous and self contradictory.  However one interprets this portion it is suggested between the lines that the authors are concerned about an emerging problem of over treatment of small filling defects, a problem that would nearly cease to exist if clinicians relied on the best evidence and chose VQ over CT scanning as the initial imaging modality to assess for PE.

A prospective observational cohort study is underway to help answer the question.


Some patients with acute PE can be treated at home.

---meaning that they can be sent straight home from the ER or sent home after only very brief (a day or so) hospitalization.  The last edition of the guidelines said that some PE patients can be sent home after a very short stay.  The current ones take it a step further to say some patients can have their entire treatment outside the hospital.  In order to be eligible the following conditions are specified in the text, all of which must be met:

1) clinically stable with good cardiopulmonary reserve; (2) no contraindications such as recent bleeding, severe renal or liver disease, or severe thrombocytopenia (ie,less than 70,000/mm 3);  (3) expected to be compliant with treatment; and (4) the patient feels well enough to be treated at home.

Note that risk scores (eg PESI), biomarkers and other clinical indicators for RV dysfunction are not included explicitly in these criteria although criterion #1 would imply that there has been some assessment of RV function and in the text the authors say that elevated biomarkers or other indicators of RV dysfunction should discourage outpatient treatment.


As in the previous edition of the guidelines, it is suggested that hypotensive PE be treated with systemic thrombolytic therapy.

---but not generally normotensive PE even when the latter is associated with RV dysfunction (aka submassive PE).  The guideline suggests that if patients with submassive PE not initially treated with thrombolysis subsequently deteriorate, even short of developing hypotension, that lysis may then be indicated.


Catheter delivered regional thrombolysis for hypotensive PE is only suggested in certain circumstances.

These are stated in the guideline thusly:

..acute PE associated with hypotension and who have (i) a high bleeding risk, (ii) failed systemic thrombolysis, or (iii) shock that is likely to cause death before systemic thrombolysis can take effect (eg, within hours)..

What about anticoagulant failure?

From the guideline text:

In patients who have recurrent VTE on VKA therapy (in the therapeutic range) or on dabigatran, rivaroxaban, apixaban, or edoxaban (and are believed to be compliant), we suggest switching to treatment with LMWH at least temporarily (Grade 2C)…

In patients who have recurrent VTE on long-term LMWH (and are believed to be compliant), we suggest increasing the dose of LMWH by about one-quarter to one-third (Grade 2C).

How is bleeding risk assessed?

Many of the recommendations and suggestions above vary with bleeding risk.  Low risk is defined as no risk factors, moderate risk is defined as 1, and 2 or more mean high.  The factors are age over 65, prior bleeding, cancer, renal failure, liver failure, thrombocytopenia, prior stroke, DM, anemia, antiplatelet therapy, poor anticoagulant control, comorbidities causing reduced functional capacity, recent surgery, frequent falls, alcohol abuse and use of nsaids. 

ACLS 2015

This has already been the subject of numerous social media posts since the guidelines were released in November.  Here I'll just comment on what I believe to be the most important changes since 2010.

The full text of the guideline issue of Circulation is here.

A new and different format for future updates.

Instead of continuing with a single update release every 5 years ACLS guidelines will now transition to a continuously updating web based format. The link to that web site is here.

Scientific advances influence ethical decision making.

The loftiest ethical principles are next to useless if not supported by appropriate scientific understanding. Put another way, many bad decisions are made not because of fundamentally bad ethics but because of a lack of understanding about what available technology will and won't do. Examples relevant to ACLS 2015 include therapeutic hypothermia and ECMO.

New upper limits of compression rate and depth.

This became necessary to deal with a manifestation of the law of unintended consequences. When word got out that we should fall on top of the chest and push hard and fast people at times got carried away. Accumulating evidence suggested that excessive rate and depth were associated with lower ROSC rates and more injury, respectively. Here's what the new guidelines have to say about it:

In adult victims of cardiac arrest, it is reasonable for rescuers to perform chest compressions at a rate of 100 to 120/min (Class IIa, LOE C-LD). The addition of an upper limit of compression rate is the result of 1 large registry study associating extremely rapid compression rates with inadequate compression depth.

During manual CPR, rescuers should perform chest compressions at a depth of at least 2 inches or 5 cm for an average adult, while avoiding excessive chest compression depths (greater than 2.4 inches [6 cm]) (Class I, LOE C-LD).

But how do you gauge your own compression depth down to tenths of an inch?

New recommendations for patients with respiratory arrest and suspected opioid abuse.

From the executive summary:

For patients with known or suspected opioid addiction who have a definite pulse but no normal breathing or only gasping (ie, a respiratory arrest), in addition to providing standard BLS care, it is reasonable for appropriately trained BLS providers to administer intramuscular or intranasal naloxone (Class IIa, LOE C-LD).

At long last the guidelines acknowledge the Arizona protocol for cardiocerebral resuscitation (CCR) but don't go far enough.

Again from the executive summary:

For witnessed OHCA with a shockable rhythm, it may be reasonable for emergency medical service (EMS) systems with priority-based, multi-tiered response to delay positive-pressure ventilation by using a strategy of up to 3 cycles of 200 continuous compressions with passive oxygen insufflation and airway adjuncts (Class IIb, LOE C-LD).

We do not recommend the routine use of passive ventilation techniques during conventional CPR for adults, because the usefulness/effectiveness of these techniques is unknown (Class IIb, LOE C-EO). However, in EMS systems that use bundles of care involving continuous chest compressions, the use of passive ventilation techniques may be considered as part of that bundle (Class IIb, LOE C-LD).

For some background on CCR read here. The first sentence of the second paragraph above is misleading. Although data in support of CCR might be considered low level by some EBM purists the evidence in the aggregate is convincing, as cited in the link above. Despite evidence of better neurologically intact survival attributable to CCR it only gets a IIb recommendation. In this particular area the guideline, in my opinion, is about a decade out of date.

Despite an emerging body of evidence for point of care ultrasound it is given only brief mention in the guidelines.

From part 7 of the guideline:

Bedside cardiac and noncardiac ultrasound are frequently used as diagnostic and prognostic tools for critically ill patients.44 Ultrasound may be applied to patients receiving CPR to help assess myocardial contractility and to help identify potentially treatable causes of cardiac arrest such as hypovolemia, pneumothorax, pulmonary thromboembolism, or pericardial tamponade.45 However, it is unclear whether important clinical outcomes are affected by the routine use of ultrasound among patients experiencing cardiac arrest.

Changes in the recommendations for vasopressin.

It has been removed from the routine algorithms but inserted in a new bundle that has a low level recommendation. Again from the executive summary:

Vasopressin was removed from the ACLS Cardiac Arrest Algorithm as a vasopressor therapy in recognition of equivalence of effect with other available interventions (eg, epinephrine). This modification valued the simplicity of approach toward cardiac arrest when 2 therapies were found to be equivalent.

BUT…

A IIb recommendation for vasopressin as part of a bundle was given for in hospital cardiac arrest. From the executive summary:

The use of steroids in cardiac arrest is controversial. In OHCA, administration of steroids did not improve survival to hospital discharge in 2 studies, and routine use is of uncertain benefit. The data regarding the use of steroids for IHCA were more vexing. In 2 randomized controlled trials led by the same investigators, a pharmacologic bundle that included methylprednisolone, vasopressin, and epinephrine administered during cardiac arrest followed by hydrocortisone given after ROSC improved survival. Whether the improved survival was a result of the bundle or of the steroid therapy alone could not be assessed. As a result of this study, in IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and postarrest hydrocortisone as described by Mentzelopoulos et al16 may be considered; however, further studies are needed before the routine use of this therapeutic strategy can be recommended (Class IIb, LOE C-LD).

The study in question is linked here.

ECMO (ECPR) is given a IIb recommendation in limited situations when expertise is available.

From part 6:

There is insufficient evidence to recommend the routine use of ECPR for patients with cardiac arrest. In settings where it can be rapidly implemented, ECPR may be considered for select patients for whom the suspected etiology of the cardiac arrest is potentially reversible during a limited period of mechanical cardiorespiratory support (Class IIb, LOE C-LD). Published series have used rigorous inclusion and exclusion criteria to select patients for ECPR. Although these inclusion criteria are highly variable, most included only patients aged 18 to 75 years, with arrest of cardiac origin, after conventional CPR for more than 10 minutes without ROSC. Such inclusion criteria should be considered in a provider’s selection of potential candidates for ECPR.

Lipid rescue (ILE) is given a IIb recommendation.

From part 10:

It may be reasonable to administer ILE, concomitant with standard resuscitative care, to patients with local anesthetic systemic toxicity and particularly to patients who have premonitory neurotoxicity or cardiac arrest due to bupivacaine toxicity (Class IIb, LOE C-EO). It may be reasonable to administer ILE to patients with other forms of drug toxicity who are failing standard resuscitative measures (Class IIb, LOE C-EO).

A multimodal approach to estimation of prognosis.

There are detailed updated recommendations for combining neuro exam findings, imaging findings, EEG findings and biomarkers in the guideline. Of interest, for intubated patients, failure to achieve an ETCO2 of greater than 10 is a negative indicator that can be combined with other findings in the estimation of prognosis.

Techniques to promote negative intrathoracic pressure and mechanical CPR devices were reviewed.

These were all either given a IIb recommendation or not recommend at all.

When PE is the cause of the arrest

From part 10:

In patients with confirmed PE as the precipitant of cardiac arrest, thrombolysis, surgical embolectomy, and mechanical embolectomy are reasonable emergency treatment options (Class IIa, LOE C-LD). Comparative data are not available to recommend one strategy over another. Patient location, local intervention options, and patient factors (including thrombolysis contraindications) are recognized elements to be considered. Thrombolysis can be beneficial even when chest compressions have been provided (Class IIa, LOE C-LD). Given the poor outcomes associated with fulminant PE in the absence of clot-directed therapy, standard contraindications to thrombolysis may be superseded by the need for potentially lifesaving intervention.

This, unfortunately, is not very helpful. In the peri-arrest situation the best opportunity for benefit with thrombolytic therapy usually comes when PE is only suspected, not confirmed. But for merely suspected PE the authors give no recommendation one way or the other, citing a lack of evidence.

Updated recommendations for post arrest evaluation and care.

An EEG is recommend for all comatose post arrest patients to diagnose possible seizure, whether or not motor activity is manifested. The guideline cites evidence that epileptiform activity, including non convulsive seizures, may have a prevalence as high as 22%. This is a class I recommendation. The recommendation for antiepileptic drugs is similar to that for status epilepticus in general.

A post arrest oxygen saturation target of 94% is recommended.

There being insufficient evidence, no blood glucose targets are recommended.

No special hemodynamic goals were recommended other than the avoidance of hypotension, meaning SBP below 90 or MAP below 65. This is a IIb recommendation.

Early cardiac catheterization is recommended for all patients in whom an acute coronary event is merely suspected, with or without ST elevation and regardless of neurologic status.

Therapeutic hypothermia is recommend for 24 hours for all post arrest patients not following commands, regardless of presenting rhythm or location of the arrest. No absolute contraindications were given. The new target is 32 to 36 C inclusive.

Defer estimation of neurologic prognosis until: 72 hours post ROSC in those not treated with hypothermia (add estimated time for sedatives and paralytics to wear off) and 72 hours post return to normothermia plus similarly added time in those treated with hypothermia. This often amounts to 4 or 5 days in hypothermia patients.